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  • What to do with all of these lung nodules? · 2018. 4. 19. · What to do with all of these lung nodules? Can Respir J Vol 21 No 3 May/June 2014 e53 The prevalence of nodules in RA
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Can Respir J Vol 21 No 3 May/June 2014 e52 What to do with all of these lung nodules? Dmitry Rozenberg MD 1,2 , Shane Shapera MD 1,2 1 Division of Respiratory Medicine; 2 Department of Medicine, University of Toronto, Toronto General Hospital, Toronto, Ontario Correspondence: Dr Dmitry Rozenberg, 9N 971 – 585 University Avenue, Toronto, Ontario M5G 2N2. Telephone 416-340-4800, fax 416-340-3254, e-mail [email protected] Learning objectives • To recognize that Caplan syndrome is a rare pulmonary manifestation of rheumatoid arthritis (RA) found in patients with occupational dust exposure. • To be aware of the differential diagnosis and management of cavitary pulmonary nodules in Caplan syndrome. CAN MEDS Competency: Medical Expert Pretest • What is the classic clinical and radiological presentation of Caplan syndrome? • What is the differential diagnosis of cavitary pulmonary nodules in RA? • How do you treat Caplan syndrome? CASE PRESENTATION A 71-year-old man was referred to the authors’ facility with a five-year history of multiple, bilateral cavitary lung nodules. He was asymptom- atic from a respiratory standpoint, with only mild dyspnea on exertion over the past six months, with no weight loss, cough or hemoptysis. The patient described a 10-year history of polyarthritis consistent with his known diagnosis of seropositive rheumatoid arthritis (RA). His RA was previously well controlled with methotrexate and leflunomide for several years. Four years before presenting to the authors’ centre, his medications were changed to azathioprine and prednisone, given the concern of multiple lung nodules (Figure 1A). He also had ischemic cardiomyopathy, atrial fibrillation, type 2 diabetes and gastroesopha- geal reflux disease. He was a retired construction worker who had significant exposure to rock dust as a result of rock drilling for 10 years and rock mining in graphite mines in the latter part of his career. He had no asbestos or sandblasting exposure. He was an ex-smoker (30 pack-year history) with no alcohol or recreational drug use. He described no tuberculosis exposures. His family history was noncontributory. On examination, the patient appeared comfortable and in no res- piratory distress. His cardiorespiratory examination was unremarkable aside from an oxygen saturation of 92% on room air. He had hand changes consistent with a diagnosis of RA with no digital clubbing. He had no subcutaneous nodules, rashes or joint swelling. His pulmonary function tests demonstrated a mixed pattern with mild restriction (total lung capacity 5.0 L [70% predicted]) and post- bronchodilator obstruction (forced expiratory volume in 1 s [FEV 1 ]/ forced vital capacity [FVC] ratio 0.67; FEV 1 1.46L [45% of predicted]) with a moderate reduction in his diffusing capacity for carbon monox- ide (DLCO) (47%). His vital capacity (VC) was 2.2 L (49%) and his residual volume 2.8 L (110%). His rheumatoid factor (>650 kIU/L) and anticitrullinated protein antibody (500 mg/L) were strongly posi- tive; antinuclear antibody, extranuclear antigen panel and antinuclear cytoplasmic antibodies were negative; and erythrocyte sedimentation rate (73 mm/h) and C-reactive protein (77 mg/L) were moderately ele- vated. His echocardiogram had shown a left ventricular ejection fraction of 40%, with no evidence of pulmonary hypertension. Chest imaging demonstrated stable calcified mediastinal and hilar lymphadenopathy with numerous parenchymal nodules and cavities, which had waxed and waned over the past five years (Figures 1A to 1C). Cultures from a spontaneous sputum sample (culture and sensi- tivity, acid-fast bacilli and fungal) were negative six months before presentation at the authors’ centre. Subsequently, bronchoscopy dem- onstrated normal anatomy, cytology and a second set of negative cul- tures (culture and sensitivity, acid-fast bacilli and fungal). A left-sided video-assisted thoracic surgical biopsy revealed multiple nodules with necrosis surrounded by dust, with areas of surrounding inflammation and fibroblastic response (Figures 2A and 2B). A diagnosis of Caplan syndrome was made. His referring physicians were advised to continue with the current extrapulmonary RA management. Tiotropium was started for his con- comitant airflow obstruction with improvement in his pulmonary function tests (total lung capacity 5.4 L [78% of predicted]; FEV 1 /FVC ratio 0.90; FEV 1 2.2 L [70%]). His VC was 2.5 L (56%), residual vol- ume 2.9 L (116%) and DLCO (58%). The nodules remain unchanged over one year of follow-up. DISCUSSION With a prevalence of approximately 1% in Canada (1), RA has many pulmonary manifestations: necrobiotic nodules, interstitial disease, pleural abnormalities, bronchiolitis obliterans, vasculitis, drug-induced lung disease, upper airway disease, organizing pneumonia and Caplan syndrome (2,3). CLINICO-PATHOLOGIC CONFERENCES ©2014 Pulsus Group Inc. All rights reserved D Rozenberg, S Shapera. What to do with all of these lung nodules? Can Respir J 2014;21(3):e52-e54. Caplan syndrome is a rare entity that is specific to rheumatoid arthritis and presents with multiple, well-defined necrotic nodules in patients with occupational dust exposure. The present report describes a case of Caplan syndrome involving a 71-year-old man with a known diagnosis of seroposi- tive rheumatoid arthritis who presented to the authors’ centre with a five- year history of multiple, bilateral cavitary lung nodules with mild dyspnea on exertion. He was an ex-smoker (30 pack-years) and had previously worked with silica. The case highlights the clinical, radiological and patho- logical features of this syndrome and outlines the importance of consider- ing a broad differential in the management of pulmonary nodules, especially in patients with rheumatoid arthritis. Key Words: Lung diseases; Nodules; Pneumoconiosis; Rheumatoid arthritis Que faire de tous ces nodules pulmonaires? Le syndrome de Caplan est une entité rare propre à la polyarthrite rhuma- toïde qui se manifeste par de multiples nodules nécrotiques bien définis chez des patients qui, à cause de leur travail, sont exposés à la poussière. Le présent rapport décrit le cas d’un homme de 71 ans atteint du syndrome de Caplan ayant un diagnostic connu de polyarthrite rhumatoïde séropositive. Il a consulté au centre des auteurs et présentait de multiples nodules pul- monaires cavitaires bilatéraux accompagnés d’une légère dyspnée à l’effort. Ancien fumeur (30 paquets-années), il avait déjà travaillé avec de la silice. Le cas fait ressortir les caractéristiques cliniques, radiologiques et pathologiques de ce syndrome ainsi que l’importance d’envisager un vaste diagnostic différentiel dans la prise en charge des nodules pulmonaires, surtout chez les patients atteints de polyarthrite rhumatoïde.

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  • Can Respir J Vol 21 No 3 May/June 2014e52

    What to do with all of these lung nodules?Dmitry Rozenberg MD1,2, Shane Shapera MD1,2

    1Division of Respiratory Medicine; 2Department of Medicine, University of Toronto, Toronto General Hospital, Toronto, OntarioCorrespondence: Dr Dmitry Rozenberg, 9N 971 – 585 University Avenue, Toronto, Ontario M5G 2N2.

    Telephone 416-340-4800, fax 416-340-3254, e-mail [email protected]

    Learning objectives• To recognize that Caplan syndrome is a rare pulmonary

    manifestation of rheumatoid arthritis (RA) found in patientswithoccupationaldustexposure.

    • To be aware of the differential diagnosis andmanagement ofcavitarypulmonarynodulesinCaplansyndrome.

    CAN MEDS Competency: Medical Expert

    Pretest• WhatistheclassicclinicalandradiologicalpresentationofCaplan

    syndrome?• Whatisthedifferentialdiagnosisofcavitarypulmonarynodules

    inRA?• HowdoyoutreatCaplansyndrome?

    CASE PrESENtAtioNA71-year-oldmanwasreferredtotheauthors’facilitywithafive-yearhistoryofmultiple,bilateralcavitarylungnodules.Hewasasymptom-aticfromarespiratorystandpoint,withonlymilddyspneaonexertionoverthepast sixmonths,withnoweight loss,coughorhemoptysis.Thepatientdescribeda10-yearhistoryofpolyarthritisconsistentwithhisknowndiagnosisofseropositiverheumatoidarthritis(RA).HisRAwaspreviouslywellcontrolledwithmethotrexateandleflunomideforseveralyears.Fouryearsbeforepresentingtotheauthors’centre,hismedicationswerechangedtoazathioprineandprednisone,giventheconcernofmultiplelungnodules(Figure1A).Healsohadischemiccardiomyopathy,atrial fibrillation, type2diabetesandgastroesopha-gealrefluxdisease.

    Hewasaretiredconstructionworkerwhohadsignificantexposuretorockdustasaresultofrockdrillingfor10yearsandrockminingingraphiteminesinthelatterpartofhiscareer.Hehadnoasbestosorsandblasting exposure.Hewas an ex-smoker (30 pack-year history)withnoalcoholorrecreationaldruguse.Hedescribednotuberculosisexposures.Hisfamilyhistorywasnoncontributory.

    Onexamination,thepatientappearedcomfortableandinnores-piratorydistress.Hiscardiorespiratoryexaminationwasunremarkableaside from an oxygen saturation of 92%on room air.Hehad hand

    changesconsistentwithadiagnosisofRAwithnodigitalclubbing.Hehadnosubcutaneousnodules,rashesorjointswelling.

    Hispulmonaryfunctiontestsdemonstratedamixedpatternwithmildrestriction(totallungcapacity5.0L[70%predicted])andpost-bronchodilatorobstruction (forced expiratoryvolume in1 s [FEV1]/forcedvitalcapacity[FVC]ratio0.67;FEV11.46L[45%ofpredicted])withamoderatereductioninhisdiffusingcapacityforcarbonmonox-ide(DLCO)(47%).Hisvitalcapacity(VC)was2.2L(49%)andhisresidualvolume2.8L (110%).His rheumatoid factor (>650kIU/L)andanticitrullinatedproteinantibody(500mg/L)werestronglyposi-tive;antinuclearantibody,extranuclearantigenpanelandantinuclearcytoplasmicantibodieswerenegative;anderythrocyte sedimentationrate(73mm/h)andC-reactiveprotein(77mg/L)weremoderatelyele-vated.Hisechocardiogramhadshownaleftventricularejectionfractionof40%,withnoevidenceofpulmonaryhypertension.

    Chestimagingdemonstratedstablecalcifiedmediastinalandhilarlymphadenopathywithnumerousparenchymalnodulesandcavities,whichhadwaxedandwanedoverthepast fiveyears(Figures1Ato1C).Culturesfromaspontaneoussputumsample(cultureandsensi-tivity, acid-fast bacilli and fungal) were negative sixmonths beforepresentationattheauthors’centre.Subsequently,bronchoscopydem-onstratednormalanatomy,cytologyandasecondsetofnegativecul-tures(cultureandsensitivity,acid-fastbacilliandfungal).Aleft-sidedvideo-assistedthoracicsurgicalbiopsyrevealedmultiplenoduleswithnecrosis surroundedbydust,withareasof surrounding inflammationandfibroblasticresponse(Figures2Aand2B).AdiagnosisofCaplansyndromewasmade.

    HisreferringphysicianswereadvisedtocontinuewiththecurrentextrapulmonaryRAmanagement.Tiotropiumwasstartedforhiscon-comitant airflow obstruction with improvement in his pulmonaryfunctiontests(totallungcapacity5.4L[78%ofpredicted];FEV1/FVCratio0.90;FEV12.2L[70%]).HisVCwas2.5L(56%),residualvol-ume2.9L(116%)andDLCO(58%).Thenodulesremainunchangedoveroneyearoffollow-up.

    DiSCuSSioNWithaprevalenceofapproximately1%inCanada(1),RAhasmanypulmonary manifestations: necrobiotic nodules, interstitial disease,pleuralabnormalities,bronchiolitisobliterans,vasculitis,drug-inducedlungdisease,upperairwaydisease,organizingpneumoniaandCaplansyndrome(2,3).

    clinico-pathologic conferences

    ©2014PulsusGroupInc.Allrightsreserved

    D rozenberg, S Shapera. What to do with all of these lung nodules? Can respir J 2014;21(3):e52-e54.

    Caplansyndromeisarareentitythatisspecifictorheumatoidarthritisandpresents with multiple, well-defined necrotic nodules in patients withoccupationaldustexposure.ThepresentreportdescribesacaseofCaplansyndromeinvolvinga71-year-oldmanwithaknowndiagnosisofseroposi-tiverheumatoidarthritiswhopresentedtotheauthors’centrewithafive-yearhistoryofmultiple,bilateralcavitarylungnoduleswithmilddyspneaon exertion. He was an ex-smoker (30 pack-years) and had previouslyworkedwithsilica.Thecasehighlightstheclinical,radiologicalandpatho-logicalfeaturesofthissyndromeandoutlinestheimportanceofconsider-ing a broad differential in the management of pulmonary nodules,especiallyinpatientswithrheumatoidarthritis.

    Key Words: Lung diseases; Nodules; Pneumoconiosis; Rheumatoid arthritis

    Que faire de tous ces nodules pulmonaires?

    LesyndromedeCaplanestuneentitérarepropreàlapolyarthriterhuma-toïde qui semanifeste par demultiples nodules nécrotiques bien définischezdespatientsqui,àcausedeleurtravail,sontexposésàlapoussière.Leprésentrapportdécritlecasd’unhommede71ansatteintdusyndromedeCaplanayantundiagnosticconnudepolyarthriterhumatoïdeséropositive.Ilaconsultéaucentredesauteursetprésentaitdemultiplesnodulespul-monairescavitairesbilatérauxaccompagnésd’unelégèredyspnéeàl’effort.Ancienfumeur(30paquets-années),ilavaitdéjàtravailléavecdelasilice.Le cas fait ressortir les caractéristiques cliniques, radiologiques etpathologiquesdecesyndromeainsiquel’importanced’envisagerunvastediagnostic différentiel dans la prise en charge des nodules pulmonaires,surtoutchezlespatientsatteintsdepolyarthriterhumatoïde.

  • What to do with all of these lung nodules?

    Can Respir J Vol 21 No 3 May/June 2014 e53

    Theprevalenceofnodules inRA isdifficult toestimate. In twooldercase seriesofRApatientswith253and702patients screenedusingchestx-ray,nonoduleswereidentified(4,5).However,onestudydemonstratedpulmonarynodulestobequitecommon,foundin13of40(32%)patientswhounderwentbiopsyforsuspectedlunginvolve-ment (6).Multiple cavitarypulmonarynodules canhavemalignantandbenignetiologies,asoutlinedinTable1.

    Inthepresentcase,malignancyandinfection(includingmycobac-terium)wasbelievedtobeunlikelygiventheindolentcourse,normal

    sputum cultures, negative bronchoscopy and video-assisted thoracicsurgicalbiopsy.AdiagnosisofCaplan syndromewasmadebasedonthe diagnostic criteria of multiple, well-defined pulmonary nodulesandinorganicdustexposureinapatientwithRA(7).Anopen-lungbiopsywasnot absolutelynecessary, butwashelpful to confirm thisrareentityandexcludealternativediagnoses.HistopathologycanbeusefulinpatientswithoutadiagnosisofRAbecausethenodulescanprecedetheonsetofRAsymptoms.

    Caplan (8) originally described this entity in 1953, havingobservedanincreasedprevalenceofpulmonarymanifestationsincoalminerswithRAwhowereexposedtomineralcoalorsilicadust.Heobservedwell-defined roundedopacities0.5cmto5cm in size thatwerebilateralandpredominantlyperipheralonchestx-ray,apatterndifferentfromprogressivemassivefibrosis(PMF),associatedwithcoalworker’s pneumoconiosis.Althoughmost cases ofCaplan syndromehave been reported in coal workers, some have been in patientsexposedtoasbestosorfreesilica(9,10),asinourcase.

    The majority of the literature regarding Caplan syndrome waspublished before the advent of chest computed tomography (CT),with relianceentirelyonchestx-rays.Althougha fewcase reportshave described using chest CT, it has not been helpful in distin-guishing Caplan syndrome from simple silicotic nodules (11,12).However,CT imaging can be useful in recognizing other forms ofRA-associatedlungdisease.Typically,radiologicalfindingsofCaplansyndromeincludebenign-appearingnodulesthatcancoalesce,cavi-tateorcalcifyintheperipheryofthelung(7).Althoughuncommon,pulmonarycomplicationscanincludepneumothorax,pleuraleffusions,hemoptysisand,mostimportantly,anincreasedprevalenceoftubercu-losiscomparedwithotherpneumoconioses(5).AmorecomprehensiveoverviewoftheclinicalandradiologicalpresentationscanbefoundinareviewarticlebySchreiberetal(7).

    Figure 1) A Computed tomography scan (coronal view) demonstrating bilateral nodules in the upper lung zones (blue arrows) and calcified hilar lymphaden-opathy (white arrows) five years before presentation. B Computed tomography scan (axial images) illustrating calcified lymph nodes (white arrows) five years before presentation. C Computed tomography scan (axial view) illustrating cavitation of the pulmonary nodules (blue arrows)

    Figure 2) A High magnification (×100) view of a necrotic nodule (star marks area of necrosis) containing abundant dust particles (arrow). Hematoxylin and eosin stain. B High magnification (×100) view of mixed dust nodule, with abundant silicotic and anthracotic dust particles (arrows), admixed with lymphohis-tiocytic cells and fibrosis (star). Hematoxylin and eosin stain

    Table 1Differential for multiple cavitary pulmonary nodulesetiology example Neoplasm Bronchogenic carcinoma (synchronous primary tumours),

    metastatic disease Infection Bacterial (Staphylococcus aureus, Klebsiella pneumoniae,

    Pseudomonas)Granulomatous (endemic fungi, mycobacterial, Nocardia)Parasitic (Paragonismus, Echinococcus)

    Inflammatory Granulomatosis with polyangitisLangerhans cell histocytosis Rheumatoid arthritisSarcoidosis

    Vascular Pulmonary embolism with infarctionPneumoconioses Berylliosis, Caplan syndrome, coal-worker’s lung, silicosis Developmental Congenital pulmonary airway malformation, pulmonary

    sequestration Drugs Amiodarone, infliximab, bleomycin, carbamazepine, othersOther Amyloidosis

  • Rozenberg and Shapera

    Can Respir J Vol 21 No 3 May/June 2014e54

    A few case reports have described pulmonary function tests inCaplan syndrome,which typicallyhave shownmild airwayobstruc-tion(7,12).Inthelargeststudytodate,however,Constantinidisetal(13)retrospectivelycompared24patientswithCaplansyndromeand36patientswithPMFsuggestingoverlapinpulmonaryfunctiontests.Whenadjustedforage,smokingandminingexposure,patientswithCaplansyndromehadlessairflowobstructionthanpatientswithPMF,butno other differenceswith respect to lung volumes anddiffusioncapacitywereidentified.Inthepresentcase,wespeculatethereducedVC and DLCO could be due to the patient’s upper lobe cavitaryfibroticchangesproducingaphysiologicalpatternoflungrestrictionthat resemblesmild PMF.Therewere no signs of diffuse interstitiallungdisease, pulmonaryvasculardiseaseorhistoryofdiaphragmaticdysfunction.

    TherehavebeentwopathologiesdescribedinCaplansyndrome,bothillustratedinourcase.Theclassicpatterninitiallydescribedin1955hasanareaofcentralnecrosisoftheRAnodulessurroundedbydustparticles.Thisarea is furthersurroundedbymultiple inflamma-torycells:neutrophils,macrophagesandseveralgiantcells(Figure2A)(14).Thesecondpatternisthesilicotictype,inwhichthenodulesaresmallerandcontainthesamefeaturesofasilicoticnodule,butmain-tainanouterringofinflammatorycellsthatisdifferentfromasimplesilicotic nodule (Figure 2B) (10). The differential for these patho-logicalfindingsincludesRAnodules,silicoticnodulesandcoalwork-er’spneumoconiosis(7).

    Despite numerous descriptions of the clinical features ofCaplansyndrome, thepathogenesisanddetailedunderstandingof the inter-actionsbetweeninhaledinorganicdustsandtheimmuneresponseinpatientswithRAhavenotbeendefined.Thereisincreasingevidencethatsilicainhalationcanbeassociatedwiththedevelopmentofauto-immune diseases such as RA, systemic sclerosis, systemic lupus ery-thematosusandantineutrophilcytoplasmicantibodyvasculitisbutitspathogenesisrequiresfurtherstudy(7).

    ThepulmonarymanifestationsofCaplansyndromedonotrequireanyspecifictherapyunlessrarecomplicationsdevelopsuchasinfec-tionorbronchopleuralfistula(15).Inafewcases,theuseofcortico-steroids has been described in slowing the progression of rapidly

    growingnodules(16).TheroleoftumournecrosisfactorinhibitorsinthetreatmentofCaplansyndromeisunknown,butworseningofRAnodules has been reported with tumour necrosis factor use (17).Treatmentshouldbefocusedonsmokingcessation, limitingoccupa-tionalexposureandcontrollingtheextrapulmonarymanifestationsoftheunderlyingRA.

    SuMMAryThepresentcasedemonstratestheclassichistorical,radiologicalandpathologicalfeaturesofCaplansyndrome,arareentity.Thecaseout-linestheimportanceofconsideringabroaddifferentialinthemanage-mentofcavitarypulmonarynodules,especiallyinpatientswithRA.Given there is no specific therapy for Caplan syndrome, the focusshouldbeonmanagementofextrapulmonaryRA.

    Post-test:• What is the classic clinical and radiological presentation of

    Caplansyndrome?Caplan syndrome can present in patients with RA and occupa-tionaldustexposure(usuallycoal)withminimalrespiratorysymp-toms.Radiologydemonstrateswell-definedroundedopacitiesthatare 0.5 cm to 5 cm in size that are bilateral and predominantlyperipheral,andcancavitateandfluctuateovertheyears.• Whatisthedifferentialdiagnosisofcavitarypulmonarynodules

    inRA?It is important to consider a broaddifferential in thework-upofcavitarypulmonarynodules(seeTable1)ensuringthatmalignancyandtuberculosisareexcluded.• HowdoyoutreatCaplansyndrome?Caplan syndromedoesnot require any particular treatment.Themanagement should be focused on treating the extrapulmonarymanifestationsofRA.

    DiSCLoSurES:Theauthorshavenofinancialdisclosuresorconflictsofinteresttodeclare.

    rEFErENCES1.CanadianArthiritisSociety,2013(AccessedMarch12,2014).

    2.TanoueLT.Pulmonarymanifestationsofrheumatoidarthritis.ClinChestMed1998;19:667-685,viii.

    3.ShannonTM,GaleME.Noncardiacmanifestationsofrheumatoiddiseaseinthethorax.JThoracImaging1992;7:19-29.

    4.PattersonCD,HarvilleWE,PierceJA.Rheumatoidlungdisease.AnnInternMed1965;62:685-97.

    5.HorlerAR,ThompsonM.Thepleuralandpulmonarycomplicationsofrheumatoidarthritis.AnnInternMed1959;51:1179-203.

    6.YousemSA,ColbyTV,CarringtonCB.Lungbiopsyinrheumatoidarthritis.AmRevRespirDis1985;131:770-7.

    7.SchreiberJ,KoschelD,KekowJ,etal.Rheumatoidpneumoconiosis(Caplan’ssyndrome).EurJInternMed2010;21:168-72.

    8.CaplanA.Certainunusualradiologicalappearancesinthechestofcoal-minerssufferingfromrheumatoidarthritis.Thorax1953;8:29-37.

    9.MorganWK.Rheumatoidpneumoconiosisinassociationwithasbestosis.Thorax1964;19:433-5.

    10. CaplanA,CowenED,GoughJ.Rheumatoidpneumoconiosisinafoundryworker.Thorax1958;13:181-4.

    11. ArakawaH,HonmaK,ShidaH,etal.ComputedtomographyfindingsofCaplansyndrome.JComputAssistTomogr2003;27:758-60.

    12. DeCapitaniEM,SchwellerM,SilvaCM,etal.Rheumatoidpneumoconiosis(Caplan’ssyndrome)withaclassicalpresentation.JBrasPneumol2009;35:942-6.

    13. ConstantinidisK,MuskAW,JenkinsJP,etal.PulmonaryfunctionincoalworkerswithCaplan’ssyndromeandnon-rheumatoidcomplicatedpneumosoniosis.Thorax1978;33:764-8.

    14. GoughJ,RiversD,SealRM.Pathologicalstudiesofmodifiedpneumoconiosisincoal-minerswithrheumatoidarthritis:Caplan’ssyndrome.Thorax1955;10:9-18

    15. HelmersR,GalvinJ,HunninghakeGW.Pulmonarymanifestationsassociatedwithrheumatoidarthritis.Chest1991;100:235-8.

    16. DaviesD.Treatmentofrapidlyprogressiverheumatoidpneumoconiosis.BrJIndMed1973;30:396-401.

    17. KekowJ,WelteT,KellnerU,etal.Developmentofrheumatoidnodulesduringanti-tumornecrosisfactoralphatherapywithetanercept.ArthritisRheum2002;46:843-4.


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